Abstract:Aim To study the protective effect of onychin against vascular endothelial cell apoptosis induced by oxida tive stress. Methods Cultured human umbilical vein endothelial cells (ECV304) were incubated for 30 min with either vehicle (DMSO), genistein or onychin before being challenged with H2O2 . Cell viability were measured by the MTT assay, and cell apoptosis was determined by flow cytometric analysis and terminal deoxynucleotidyl transfersas-mediated dUTP nick end-labeling (Tunel) respectively. Meanwhile, Western blot was used to measure the activation of caspase-3. Results H2O2 treatment for 24 h evoked endolhelium apoptosis, and onychin (0.3, 1 and 3 μmol/L.) decreased the rate of apoptoic endothelial cells (15. 5%±1.2%, 12.6% ±0.9% and 8.2% ±0.8% vs 22.7% ± 3.9% )in a concentration-dependent manner. Meanwhile, Onychin decreased the expression of active caspase-3 induced by H2O2 as genistein. Conclusion onychin prevents H2O2-in-duced endothelium apoptosis which correlated with inhibition of caspase-3 activation.

Abstract:Aim To study the protective effects of Onychin on vasular endothelium-dependent relaxation relaxation damage induced by lysophophatidylcholine(LPC). Methods The vasorelaxation responseto acetylcholine(ACh)were investigation in the rabbit thoracic aorta; The LDH level in conditioned media of cultured endothelial cells was measured by DGKC assay. Results On the rabbit aortic rings, Onychin alone did not have effect on relaxation response to Ach and on contraction response to phenylephrine. LPC 4 mg/L significantly attenuated the endothelium-dependent relaxation of rabbit aortic rings as shown by decreasing the relaxation percentage from 39.1±10.1, 67.1±9.6 and 76.7±10.0 to 2.1±1.0, 10.0±3.9 and 16.1±3.5 response to 0.1, 1.0 and 3.0 μmol/L ACh, respectively; Pretreatment of onychin 3 μmol/L for 10 min markedly increase the relaxation percentage to 14.6±2.6,32.2±2.8,42.1±8.0. The effect of Onychin was blocked by nitric oxide synthase inhibitor N ω-nitro-L-arginine(N-L-A) and prostacyclin synthetase inhibitor indomethacin ( maximal relaxalion percentage: 22.4±7.2, 24.8±2.3 vs 42.1±7.9 to ACh 3 μmol/L). Furthermore,Onychin obviously decreased LPC-induced LDH release of cultured endothelial cells as shown by lowering LDH level from 115.3±19.3 to 30.8±5.4 IU/L. Both N-L-A and indomethacin also inhibited the effect of onychin on LDH release. Conclusion Onychin protects the endothelium-dependent relaxation against elicited-LPC injury with a mechanism related to the activation of nitric oxide and prostacyclin.